CONTRIBUTION OF THE FETAL ADRENAL TO CIRCULATING IMMUNOACTIVE INHIBININ THE CHICKEN-EMBRYO

Citation
L. Rombauts et al., CONTRIBUTION OF THE FETAL ADRENAL TO CIRCULATING IMMUNOACTIVE INHIBININ THE CHICKEN-EMBRYO, Biology of reproduction, 51(5), 1994, pp. 926-933
Citations number
35
Categorie Soggetti
Reproductive Biology
Journal title
ISSN journal
00063363
Volume
51
Issue
5
Year of publication
1994
Pages
926 - 933
Database
ISI
SICI code
0006-3363(1994)51:5<926:COTFAT>2.0.ZU;2-1
Abstract
High concentrations of immunoactive inhibin are observed in the plasma of male and female chicken embryos. The exact nature and the source o f this material remain obscure. In a previous study we presented evide nce that the fetal gonads are unlikely to be the main source of circul ating inhibin (Biol Reprod 1993; 43:543-554). Here we demonstrate that the fetal adrenal may account for the major portion of circulating im munoactive inhibin in the chicken embryo. A comparison of the inhibin content of different fetal organs shows that, expressed per milligram of tissue, the adrenal ranks second. Only the testis has a higher inhi bin content while the inhibin content of the fetal ovary is considerab ly lower than that of the fetal adrenal. Suppression of endogenous ACT H secretion by administration of dexamethasone results in a marked dec rease of plasma inhibin. Maximal suppression (down to 24% and 25% of t he control values in male and female embryos, respectively) was observ ed with the lowest dose of dexamethasone tested (1 mu g/egg). Dexameth asone (100 mu g/egg) reduced testicular weight and testicular inhibin content to approximately 50% of the control value. It is unlikely, how ever, that this contributed significantly to the fall in circulating i mmunoactive inhibin. In fact, ovarian inhibin content was unaffected, but even so, a comparable drop in circulating inhibin was observed in female embryos. Dexamethasone caused only marginal changes in plasma F SH. Administration of a syn thetic peptide with ACTH activity (Synacth en) in vivo did not produce measurable changes in circulating inhibin. Isolated and cultured fetal adrenal cells, however, produced Immunoac tive inhibin, and this production was increased fivefold after stimula tion with synthetic ACTH. Taken together, these data suggest that the adrenal is the major source of immunoactive inhibin in the chicken emb ryo. The exact nature of the adrenal inhibin and its endocrine and/or paracrine role warrant further investigation.